Expression Changes of Genes Related to Germination Based on EST Database under Priming Treatment by Gibberellic Acid in Perilla frutescens (Korean Perilla)

It is very important to establish an optimal seed priming process in order to increase the vitality of the seeds and promote the metabolism for the germination of the seeds. The optimum concentrations and species of priming agents to improve seed germination of both medicinal plants were also estimated. To improve the germination rate of Perilla frutescens(Korean perilla) seeds, various seed priming agents were used to analyze seed germination rates in the Saeyeopsil, Okdong and 141 collection Korean perilla cultivars. The agents used for seed priming were CaCl2, Ca(NO3)2, NaCl, K3PO4, polyethylene glycol, and gibberellic acid (GA3). When 0.1 mMGA3was used for seed priming, germination rates of Okdong, and the 141 collection showed a greater than 70% increase compared to the controls. Nine genes were selected for expression analysis by searching for genes related to seed germination and plant development in the EST(Expressed Sequence Tag) database of the Korean perilla cDNA library. GA3priming treatment for 1 d induced higher transcriptional levels of genes related to germination and plant developmentthan controls treated with water only. These genes were identified as protochlorophyllide reductase-like, magnesium-chelatase subunit ChlI, heme-binding protein 2-like, glyceraldehyde 3-phosphate dehydrogenase A, Chlorophyll a-b binding protein 6, B2 protein, 2-Cys peroxiredoxin BAS1, and 21 kDa protein. From these results, we suggest that when priming Korean perilla seeds with GA3, a large number of genes involved in plant development at early stages of seed germination play a role in improving the seed germination rate. Also, these induced genes are ideal candidate biomarkers for seed priming of Korean perilla. Specially, protochlorophyllide reductase-like is thought to be a potential gene for future molecular marker.© 2021 Friends Science Publishers

Comparative Plastid Genomics of Cryptomonas Species Reveals Fine-Scale Genomic Responses to Loss of Photosynthesis

Loss of photosynthesis is a recurring theme in eukaryotic evolution. In organisms that have lost the ability to photosynthesize, nonphotosynthetic plastids are retained because they play essential roles in processes other than photosynthesis. The unicellular algal genus Cryptomonas contains both photosynthetic and nonphotosynthetic members, the latter having lost the ability to photosynthesize on at least three separate occasions. To elucidate the evolutionary processes underlying the loss of photosynthesis, we sequenced the plastid genomes of two nonphotosynthetic strains, Cryptomonas sp. CCAC1634B and SAG977-2f, as well as the genome of the phototroph Cryptomonas curvata CCAP979/52. These three genome sequences were compared with the previously sequenced plastid genome of the nonphotosynthetic species Cryptomonas paramecium CCAP977/2a as well as photosynthetic members of the Cryptomonadales, including C. curvata FBCC300012D. Intraspecies comparison between the two C. curvata strains showed that although their genome structures are stable, the substitution rates of their genes are relatively high. Although most photosynthesis-related genes, such as the psa and psb gene families, were found to have disappeared from the nonphotosynthetic strains, at least ten pseudogenes are retained in SAG977-2f. Although gene order is roughly shared among the plastid genomes of photosynthetic Cryptomonadales, genome rearrangements are seen more frequently in the smaller genomes of the nonphotosynthetic strains. Intriguingly, the light-independent protochlorophyllide reductase comprising chlB, L, and N is retained in nonphotosynthetic SAG977-2f and CCAC1634B. On the other hand, whereas CCAP977/2a retains ribulose-1,5-bisphosphate carboxylase/oxygenase-related genes, including rbcL, rbcS, and cbbX, the plastid genomes of the other two nonphotosynthetic strains have lost the ribulose-1,5-bisphosphate carboxylase/oxygenase protein-coding genes.